A myosin regulatory light chain is one of the subunits constituting a multi-subunit protein product, myosin. It is known that myosin is a hexamer formed by two heavy chains, two regulatory light chains, and two essential light chains, and is a motor protein that causes actin filament contraction by using energy generated by hydrolyzing adenosine triphosphate (hereinafter abbreviated as ATP). All myosin light chains are members of calmodulin superfamily. Myl9, Myl12a, and Myl12b are known as the myosin regulatory light chain and Myl6 is known as the myosin essential light chain.
CD69 is a type II transmembrane protein belonging to C-type lectin family. CD69 is widely used as an indicator of lymphocyte activation as an early activation marker molecule because the expression level is increased within a few hours after stimulating T cells or B cells (Non Patent Literature 1). In addition, CD69 is found to be expressed also in T cells at a selection stage during differentiation in thymus gland (Non Patent Literatures 2 and 3). Further, it has been reported that CD69 is also expressed in memory CD4 T cells being maintained in bone marrow and CD69 is important for migration of activated CD4 T cells to bone marrow and subsequent maintenance of memory CD4 T cells (Non Patent Literature 4). It is supposed that CD69 has a function to enhance signaling from an antigen receptor as a coreceptor, but details thereof are unclear. The ligand of CD69 has not been identified yet. CD69 is constitutively expressed in platelets and is also expressed in activated neutrophils, eosinophils, and the like, and therefore it is supposed that CD69 has a role in functional expression of platelets and local inflammatory responses. In addition, it is revealed that CD69 on neutrophils plays a key role in development of arthritis (Non Patent Literature 5). It has also been reported that CD69 on CD4 T cells controls allergic airway inflammation and the antibody to CD69 suppresses allergic airway inflammation (Non Patent Literature 6). In addition, it has been reported that in CD69-deficient mice, COPD induced by cigarette smoke and lung fibrosis induced by bleomycin are attenuated (Non Patent Literatures 7 and 8).